Vasodilatory effects of cinnamaldehyde and its mechanism of action in the rat aorta

Yong-Liang Xue¹, Hai-Xia Shi¹, Ferid Murad^1,2, Ka Bian^1,2
1Murad Research Institute for Modernized Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, People’s Republic of China; ²E-Institute of Shanghai Universities, Division of Nitric Oxide and Inflammatory Medicine, Shanghai, People’s Republic of China

Abstract: The vasodilatory effect of cinnamaldehyde was investigated for its mechanism of action using isolated rings of rat aorta. Cinnamaldehyde relaxed aortic rings precontracted with phenylephrine in a dose-dependent manner, was not affected by either the presence or removal of the endothelium. Pretreatment with NG-nitro-L-arginine methyl ester and 1H-[1,2,4]-oxadiazole-[4,3-a]-quinoxalin-1-one could not block vasodilation by cinnamaldehyde, indicating that nitric oxide signaling is not involved. Potassium channel blockers, such as glibenclamide, tetraethylammonium, and BaCl₂, had no effect on the relaxation produced by cinnamaldehyde. In addition, treatment with either indomethacin or propranolol did not affect cinnamaldehyde-induced vasodilatation. On the other hand, pretreatment of endothelium-denuded rings with cinnamaldehyde significantly inhibited vasoconstriction induced by endogenous vasoconstrictors, including angiotensin II, 5-hydroxytryptamine, dopamine, endothelin-1, and phenylephrine. In a Ca²⁺-free experimental setting, this natural vasodilator not only blocked Ca²⁺ influx-dependent vasoconstriction by either phenylephrine or KCl, but also inhibited phenylephrine-induced tonic contraction, which relies on intracellular Ca²⁺ release. This study shows that endothelium-independent, Ca²⁺ influx and/or an inhibitory release mechanism contributes to the vasodilatory effect of cinnamaldehyde.

Keywords: cinnamaldehyde, vasodilation, endothelium, vascular smooth muscle cell